DESCRIPTION (the applicant's description verbatim): Although, there has been much progress in the management of myocardial ischemia, myocardial infarction remains the major cause of death in the U.S. Acute myocardial infarction is commonly caused by thrombosis or occlusion of the coronary arteries which feed the left ventricle of the heart. The absence of blood flow to the cardiac muscle results in severe cellular damage that eventually compromises the muscle's ability to contract. This is due, among other things, to the limitation in oxygen delivery that reduces mitochondrial oxidative phosphorylation and contributes to the reduction of intracellular ATP levels. Research has shown that the inability of the mitochondria to self-repair following restoration of blood flow may be a crucial event leading to myocardial cell death. Recent studies show that part of this myocardial cell death is through apoptosis. One of the main protein assembly structures in the mitochondria is made up by the molecular chaperones or mitochondrial stress proteins. These proteins are known as the mitochondrial hsp70, hsp60 and hsp10. These last two proteins form the chaperonin complex which together with ATP is involved in the assembly of the majority of the mitochondrial proteins including the enzyme complexes involved in oxidative phosphorylation. We have found that increased expression of the hsp60 and hsp10 in cardiomyocytes renders the myocyte significantly tolerant to ischemic injury Interestingly, we find that part of this protection effect of overexpressing the mitochondrial stress proteins is due to a reduction in the amount of apoptosis induced by ischemia/reperfusion We find that the protective effect by hsp60 and hsp10 seems to be mediated by their binding to cytochrome c and the retention of this last protein inside the mitochondria and therefore potentially decreasing the activation of the caspases, the main culprits of apoptosis We therefore believe that a better understanding of the mechanism of how the mitochondrial hsps protect the cardiomyocyte during ischemia/reperfusion injury will permit us to harness this endogenous defense mechanism